Ross J. Simpson

Age, race, and sex differences in autonomic cardiac function measured by spectral analysis of heart rate variability—The ARIC study

To investigate the distribution of heart rate variability (HRV) spectral power in an unselected sample of the population, and to ascertain the population correlates of HRV, we examined 1,984 healthy persons, aged 45 to 64 years, randomly selected from the Atherosclerosis Risk in Communities (ARIC) study cohort. Resting, supine, 2-minute, beat-to-beat heart rate data were collected between 7 A.M. and 12 noon. The race- and sex-adjusted geometric means of low-frequency component (LF, 0.025 to 0.15 Hz) were 4.00 and 3.13 (beats/min)2; of high-frequency component (HF, 0.16 to 0.35 Hz), 1.65 and 1.21 (beats/min)2; and of the HF/LF ratio, 0.41 and 0.39, for 45-to-54 and 55-to-64 years age groups, respectively (test of mean difference by age, p < 0.01, p < 0.01, and p = 0.11 for LF, HF, and HF/LF ratio, respectively). Comparing black with white examinees, the age- and sex-adjusted geometric means of LF were 3.06 and 3.70 (beats/min)2; of HF, 1.66 and 1.36 (beats/min)2; of HF/LF, 0.54 and 0.37, respectively (test of mean difference by race, p < 0.01, p < 0.01, and p < 0.01). The age- and race-adjusted geometric means of LF for women and men were 3.12 and 4.10 (beats/min)2; of HF, 1.46 and 1.38 (beats/min)2; and of HF/LF, 0.47 and 0.34, respectively (test of mean difference, p < 0.01, p = 0.34, and p < 0.01). We conclude that HRV spectral indexes are associated with age, race, and sex. With increasing age, the parasympathetic and sympathetic spectral power components decrease.(ABSTRACT TRUNCATED AT 250 WORDS)

Combination Therapy Improves Survival After Acute Myocardial Infarction in the Elderly with Chronic Kidney Disease

Background: Individuals with chronic kidney disease have a high mortality rate after acute myocardial infarction. It is not known how frequently these individuals are prescribed combination cardioprotective therapy and if survival is affected by such therapy after acute myocardial infarction. Methods: A retrospective cohort study of 1,342 Medicare recipients with acute myocardial infarction. Data were collected by medical chart abstraction as part of the Cooperative Cardiovascular Project in 60 hospitals in North Carolina during 5/30/1996–12/28/1997. We categorized cardioprotective medication use as aspirin alone, aspirin with beta‐blockers, and aspirin with beta‐blockers and ace‐inhibitors. Chronic kidney disease was defined as a derived glomerular filtration rate (GFR) ranging from 15–89 mL/min/1.73 m2. Cox proportional hazards regression analyses were performed to determine the effect of cardioprotective medication use on survival while controlling for potential explanatory variables. Results: The prevalence of cardioprotective medication use differed among levels of chronic kidney disease. Those with severe kidney disease (GFR 15–29 mL/min/1.73 m2) were less frequently prescribed aspirin with beta‐blockers, 27.1%, and only 8.6% were prescribed aspirin with beta‐blockers and ace‐inhibitors. Survival was improved with prescribed cardioprotective medication use. In severe kidney disease (GFR 15–29 mL/min/1.73 m2), the hazards risk for death was 0.21 (0.08, 0.53) for aspirin alone, 0.17 (0.06, 0.51) for aspirin with beta‐blockers, and 0.35 (0.09, 1.42) for aspirin with beta‐blockers and ace‐inhibitors. Conclusions: Individuals with chronic kidney disease benefit from combination cardioprotective therapy, but are less likely to be prescribed them after acute myocardial infarction. Further investigation is warranted to identify possible reasons for these observed treatment disparities.

Comparative Assessment of Medical Resource Use and Costs Associated with Patients with Symptomatic Peripheral Artery Disease in the United States.

BACKGROUND There is growing concern about appropriate disease management for peripheral artery disease (PAD) because of the rapidly expanding population at risk for PAD and the high burden of illness associated with symptomatic PAD. A better understanding of the potential economic impact of symptomatic PAD relative to a matched control population may help improve care management for these patients. OBJECTIVE To compare the medical resource utilization, costs, and medication use for patients with symptomatic PAD relative to a matched control population. METHODS In this retrospective longitudinal analysis, the index date was the earliest date of a symptomatic PAD record (symptomatic PAD cohort) or any medical record (control cohort), and a period of 1 year pre-index and 3 years post-index was the study time frame. Symptomatic PAD patients and control patients (aged ≥ 18 years) enrolled in the MarketScan Commercial and Encounters database from January 1, 2006, to June 30, 2010, were identified. Symptomatic PAD was defined as having evidence of intermittent claudication (IC) and/or acute critical limb ischemia requiring medical intervention. Symptomatic PAD patients were selected using an algorithm comprising a combination of PAD-related ICD-9-CM diagnostic and diagnosis-related group codes, peripheral revascularization CPT-4 procedure codes, and IC medication National Drug Code numbers. Patients with stroke/transient ischemic attack, bleeding complications, or contraindications to antiplatelet therapy were excluded from the symptomatic PAD group but not the control group. A final 1:1 symptomatic PAD to control population with an exact match based on age, sex, index year, and Charlson Comorbidity Index (CCI) was identified. Descriptive statistics comparing patient demographics, comorbidities, medical resource utilization, cost, and medication use outcomes were generated. Generalized linear models were developed to compare the outcomes while controlling for residual difference in demographics, comorbidities, pre-index resource use, and pre-index costs. RESULTS 3,965 symptomatic PAD and 3,965 control patients were matched. In both cohorts, 54.7% were male, with a mean age (SD) of 69.0 (12.9) years and a CCI score of 1.3 (0.9). Symptomatic PAD patients had more cardiovascular comorbidities than control patients (27.7% vs. 12.6% coronary artery disease, 27.1% vs. 15.9% hyperlipidemia, and 49.8% vs. 28.2% hypertension) in the pre-index period. Post-index rates of ischemic stroke, non-ST segment elevation myocardial infarction, unstable angina, and cardiovascular- or PAD-related procedures (limb amputations, endovascular procedures, open surgical procedures, percutaneous coronary intervention, and coronary artery bypass graft) were higher among symptomatic PAD patients versus control patients. All-cause annualized inpatient admissions (0.46 vs. 0.22 admissions), emergency department/urgent care days (0.27 vs. 0.22 days), and office visit days (12.5 vs. 10.2 days) were higher among symptomatic PAD versus control patients post-index. Annualized all-cause inpatient costs (

Additional evidence for re-entry within the bundle branches in man.

8,494 vs.

Resource use and costs in high-risk symptomatic peripheral artery disease patients with diabetes and prior acute coronary syndrome: a retrospective analysis

3,778); outpatient costs (

Classifying medical histories in US Medicare beneficiaries using fixed vs all-available look-back approaches

8,459 vs.

Does Cholesterol Reduction with Cholestyramine Prevent Coronary Heart Disease among Individuals with Prehypertension

5,692); and total costs (

Lipid Profiles in Out-of-Hospital Sudden Unexpected Death

20,880 vs.

Medication Use in Women and Men With Sudden Unexpected Death

12,501) were higher among symptomatic PAD versus control patients post-index. Only 17.8% of symptomatic PAD patients versus 6.6% of control patients were on clopidogrel pre-index. In the post-index period, clopidogrel prescriptions in the symptomatic PAD population increased to 38.0%. Results were consistent in the regression models with the symptomatic PAD population having a higher number of all-cause post-index inpatient admissions, emergency department/urgent care days, office visit days, inpatient costs, outpatient costs, and total costs versus control patients (P ≤ 0.026). CONCLUSIONS Symptomatic PAD patients have significantly higher medical resource use and costs when compared with a matched control population. As the prevalence of symptomatic PAD increases, there will be a significant impact on the population and health care system. The rates of use of evidence-based secondary prevention therapies, such as antiplatelet medication, were low. Therefore, greater effort must be made to increase utilization rates of appropriate treatments to determine if the negative economic and clinical impacts of symptomatic PAD can be minimized. DISCLOSURES This study was funded by Merck & Co., Kenilworth, New Jersey. Chase and Heithoff are employees of Merck & Co., Kenilworth, New Jersey, and Upper Gwynedd, Pennsylvania. Friedman and Navaratnam are paid consultants for Merck & Co. Simpson is a paid consultant for Merck, Pfizer, and Amgen and has received speakers fees from Merck and Pfizer. Study concept and design were contributed by Chase, Navaratnam, and Heilhoff, along with Simpson and Friedman. Friedman collected the data, which was interpreted by Simpson and Navaratnam, along with Friedman. The manuscript was written by Navaratnam and Friedman, along with Chase, Heilhoff and Simpson, and revised by all of the authors.

Antiplatelet Therapy and Clinical Outcomes Following Myocardial Infarction Among Patients in a U.S. Employer-Based Insurance Database

A repetitive, non‐paced ventricular beat (V3) often occurs during ventricular extrastimulus testing at short coupling intervals when critical retrograde His‐Purkinye conduction delay is achieved. Though re‐entry within the bundle, branches has been proposed as the mechanism for V3. it has been difficult to exclude local re‐entry. In the present case, we consistently recorded a right bundle branch potential as well as a bundle of His potential before each V3. The anterogrude activation sequence of these potentials provides evidence against local reentry and supports re‐entry involving the bundle branches as the mechanism for V3.